TCDs, SAH, HHH VERY LONG
- 0May 8, '06 by ParrotHeadRNI worked the last three nights. My first night I picked up a SAH in her mid 30's, no hx but migraines. She went down for a coiling and came back that night fine. Her pressures were a little low, but she was intact. That morning the neurosurgeon came in and said he was going to address her pain (HA refractory to meds) and her pressure, so I left feeling good. The next night when I had her, she was still intact, but her pressures were still low, like in the 90s-100s. I called the intensivist twice about her pressures. The first time he said to bolus her, which did no good, and the second time he said that since she was intact to just watch her. I was having serious concerns at that time because even though she was intact, she had had a BIG bleed, including IVH and I knew she was going to spasm. I should add that despite the size of her bleed, she presented with a Hunt and Hess of II/IV. PLUS I knew her pressures were also low because she was getting a BOATLOAD of pain meds for severe unrelenting HA AND the nimodipine was dropping her pressure as well, even when I gave it 1 q 2h. Why were we not doing HHH on her?
SO, when I arrived last night, low and behold, the TCDs had shown SEVERE spasming and she now had a swan, an a line, and was on neo. THANK god. I also quite honestly felt I had not done enough in being an advocate for the pt and had decided that when I went back last night I was going to raise heck if the situation was still the same. Luckily, it wasn't. AND they did an LP. Her CSF was bloody, her WC, RC, and protein were through the roof and her glucose was 29. Sounds like....meningitis??? Hmmm. However, her serum WBC were 13, and she was afebrile.
Last night around 2100 she became a little lethargic/confused and started having a mild drift. I was already titrating up the neo, but I cranked it up more (we were shooting for a MAP of 110 and she was having a hard time getting there.) The intensivist was present and I discussed the situation w/ him. We were both in agreement that her pressures needed to go up and that she was getting lots of pain meds. So I watched her all night and continued cranking up her neo. By this morning she was at 150 mcgs. AND she was intact again, no drift, alert. Her MAP was 110-120. I had continued to give her pain medicine all night so I deduced that the pain meds were NOT making her confused as that had not changed. I felt I had done a good job that night of taking care of her, was pretty satisfied although exhausted. I was concerned that her WC was up to 17, NO atb tx, and she had started to c/o nuccal rigidity.
The neurosurgeon came in this morning with his intern/resident whatever and started throwing it around that she WASN'T spasming and basically laughing at the intensivist for everything he had done, which in turn I felt he was being condescending to me as well. He wanted to know who told me she was spasming. I replied that her nurse the day before had as well as the TCD report. As I was trying to explain what had happened the night before, he was too busy talking over me about how she's okay and doesn't need HHH and we need to titrate the neo off. The words ran right out of my mouth before I could even think. "you better not!" Of course, he didn't like that, but mostly just laughed about it with his groupies. Then he wanted to know who was taking care of her that day. I told him and he said "okay that's great." I also tried to tell him about her nuccal rigidity and he said it was from blood in the subarachnoid space. Which is fine, but w/ everything else....
When I was giving report, the nurse rec'ing said the surgeon had stopped her in the hall and said "she's not spasming, don't let anybody tell you otherwise." Who could he have been talking about???
And apparently he had at some point said she didn't have a SAH, she had bleeding in the basal ganglia. Ok, but she was coiled AND he told me she had blood in her subarachoid space.
So, the orders today from him were to titrate neo OFF w/ no parameters. And he was such a condescending jerk. My biggest concern though is that I feel this pt, who is very young, is going to be grossly mismanaged if indeed her pressors are weaned off.
I know this is so long, so I'll try to wrap it up. I know I have only been in NSICU for two years, so I am asking all of you what you think. Are TCDs NOT indicative of spasming and if not, WHY are we doing them? Am I totally wrong in my thinking? Is there something I don't know? I am really upset about this from start to finish. If there was something to teach me, this would have been the perfect opportunity for him to do so, but he instead chose to make a mockery not only of me and my practice but another doctor as well, and in front of other people. But again, the big issue is the patients care. What can you guys tell me?
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- 0May 8, '06 by leggendarioYeah in this kind of situation wherein a nurse suspect something is happening to the patient that is different from the current diagnosis of the AP's. In this case the dilemma is that you are suspecting that the patient is suffering from meningitis and not from SAH.
I have a similar experience which is in the opposite direction as this one. My patient was diagnosed to have an acute bacterial meningitis but was not showing any signs of pathological hallmark of meningitis. There is no nuchal, the patient is Afebrile and slight hypertensive 130/80 - 140/90. It undergoes CT-SCan and reveal nothing but atrophy of certain parts of the brain which is brought by aging. By the way my patient was already 71 years old male.
To my surprise he was given 3 million units of Pen G every 4 hours, Mannitol to relieve ICP. Dexamethasone to relieve the cerebral edema, and citicholine every 8 hours. He had to AP's one AP is an Internist and one is a Neurologist. Given the fact that the only diagnostic test that they done to the patient other than the lab which shows his Hgb at normal level 13.3 and an elevation in WBC 16.6 1 they made a conclusive diagnosis of acute bacterial meningitis. I was suprised that they did not do any lumbar puncture to strengthen their position regarding the diagnosis of this patient.
I received the patient of having only a Glasgow Coma Scale of 3, then after several hours his level of sensorium improved to GCS 6 then to 8. He started to have a spontaneous eye opening and spontaneous movement.
Then later on after several days with the same regimen the patient regains his consciousness and shows some signs of left sided hemiparesis.
Although looking at the given data of the patient I think the AP's are hitting a single target with 2 bullets. I suspect that the AP's was not certain if the patient is really suffering from Meningitis or Cerebral Infarct which I think the latter is the main cause of his Loss of Consciousness.
Just my 2 cents.
- 0May 9, '06 by RoxanRN2003Quote from parrotheadrnmy opinion is that this doctor should be written up for unprofessional conduct. it is so not professional to talk crap about a fellow physician's work in front of other people - whether they agree with the treatment or not. he needs to take it up directly with the other doctor.if there was something to teach me, this would have been the perfect opportunity for him to do so, but he instead chose to make a mockery not only of me and my practice but another doctor as well, and in front of other people. but again, the big issue is the patients care. what can you guys tell me?
in my unit (neuro critical care), this condescending jerk would have been written up and reported to our unit manager. in turn, she would take the matter up with the neuro intensivest/unit's medical director concerning nursing concerns about the course of treatment (we nurses aren't as stupid some doctors want/hope us to be) and (hopefully) would talk with the offensive physician about his attitude.
oh, and just as a matter of course, our surgeons generally turn care of the patient over to the unit's neuro intensivests. it is extremely rare that the surgeon will come in and counter the intensivest.
- 0May 10, '06 by JennyMacRN2BI think TCD's are good tool to evaluate vasospasm. Besides doing an arteriogram and neuro changes, it is truly the only tool we have. If the velocities have increased from the baseline, then it is indication that the vessels are getting smaller. Of course I am not a neurosurgeon, but that only makes sense. Luckily in my unit we have a vasospasm protocol that all the docs follow with a SAH. For instance, your patient in our unit would be on neo or dopamine with parameters SBP 160-180 (secured aneurysm). Of course after a few days with no neuro changes these can be relaxed. Of course it does take a few days for vasospasm to occur. I would worry if I had a patient with a SAH that was not having a bad headache. I think its just the nature of the beast.
Of the neurosurgeons, he was just being a jerk, but with that too, I think is just the nature of the beast.
- 0May 13, '06 by JennyMacRN2BTCD's are transcranial dopplers, they use them to measure the velocity of the blood flowing through the circle of willis vessels in order to detect vasospasm
HHH therapy is hemodilution, hypertension and hemodynamics (I think that last one is right). It is used with a SAH to keep blood volumes up and pumping through those vessels that might close off due to vasospasm, causing a lack of blood flow o the brain.
- 0Jun 9, '06 by auzzieneuronurseWell Done!! You fought hard for the best outcome for your patient and should have been treated with the respect you deserve!!!! Listen to your instincts! Some neurosurgeons don't think TCD's hold much weight but with her clinical signs it would have to be a cert wouldn't it????
Did they do a repeat CTB to check for communicating hydocephalus which may also have contributed to her confusion?? (I assume they didn't have an EVD in if they had to do a LP.)
p.s. the third H is for hypervolemia not haemodynamics